A predicted in vivo muscle force – velocity trajectory

1997 ◽  
Vol 75 (3) ◽  
pp. 371-375 ◽  
Author(s):  
J.-Y. Cheng ◽  
M. E. DeMont

The in vivo stress–strain and stress – strain rate relationships of the adductor muscle in a swimming scallop (Placopecten magellanicus) were predicted on the basis of detailed measured swimming movements and a recently developed dynamic model that integrates all important mechanical elements in the process. The in vivo behaviour of the muscle was found to be quite different than the in vitro properties measured on isolated muscle fibres, which suggests that in general the latter might not be directly used to predict the in vivo mechanical events.

2018 ◽  
Author(s):  
Yihua Wang ◽  
Katalin Ajtai ◽  
Thomas P. Burghardt

ABSTRACTNative cardiac ventricular myosin (βmys) translates actin under load by transducing ATP free energy into mechanical work on actin during muscle contraction. Unitary βmys translation of actin is the myosin step-size. In vitro and in vivo βmys regulates contractile force and velocity by remixing 3 different step-sizes with stepping frequencies autonomously adapted to workload. Cardiac and skeletal actin isoforms have a specific 1:4 stoichiometry in normal adult human ventriculum. Human adults with inheritable hypertrophic cardiomyopathy (HCM) up-regulate skeletal actin in ventriculum suggesting that increasing skeletal/cardiac actin stoichiometry also adapts myosin force-velocity to respond to the muscle’s inability to meet demand.Nanometer scale displacement of quantum dot (Qdot) labeled actin under resistive load when impelled by βmys measures single myosin force-velocity in vitro in the Qdot assay. Unitary displacement classification constraints introduced here better separates myosin based signal from background upgrading step-size spatial resolution to the sub-nanometer range. Single βmys force-velocity for skeletal vs cardiac actin substrates was compared using the Qdot assay.Two competing myosin strain-sensitive mechanisms regulate step-size choices dividing mechanical characteristics into low- and high-force regimes. The actin isoforms alter myosin strain-sensitive regulation such that onset of the high-force regime, where a short step-size is a large or major contributor, is offset to higher loads by a unique cardiac ELC N-terminus/cardiac-actin contact at Glu6/Ser358. It modifies βmys force-velocity by stabilizing the ELC N-terminus/cardiac-actin association. Uneven onset of the high-force regime for skeletal vs cardiac actin dynamically changes force-velocity characteristics as skeletal/cardiac actin fractional content increases in diseased muscle.


1993 ◽  
Vol 265 (6) ◽  
pp. L549-L554 ◽  
Author(s):  
R. W. Mitchell ◽  
I. M. Ndukwu ◽  
K. Arbetter ◽  
J. Solway ◽  
A. R. Leff

We studied the effect of either 1) immunogenic inflammation caused by aerosolized ovalbumin or 2) neurogenic inflammation caused by aerosolized capsaicin in vivo on guinea pig tracheal smooth muscle (TSM) contractility in vitro. Force-velocity relationships were determined for nine epithelium-intact TSM strips from ovalbumin-sensitized (OAS) vs. seven sham-sensitized controls and TSM strips for seven animals treated with capsaicin aerosol (Cap-Aer) vs. eight sham controls. Muscle strips were tethered to an electromagnetic lever system, which allowed isotonic shortening when load clamps [from 0 to maximal isometric force (Po)] were applied at specific times after onset of contraction. Contractions were elicited by supramaximal electrical field stimulation (60 Hz, 10-s duration, 18 V). Optimal length for each muscle was determined during equilibration. Maximal shortening velocity (Vmax) was increased in TSM from OAS (1.72 +/- 0.46 mm/s) compared with sham-sensitized animals (0.90 +/- 0.15 mm/s, P < 0.05); Vmax for TSM from Cap-Aer (0.88 +/- 0.11 mm/s) was not different from control TSM (1.13 +/- 0.08 mm/s, P = NS). Similarly, maximal shortening (delta max) was augmented in TSM from OAS (1.01 +/- 0.15 mm) compared with sham-sensitized animals (0.72 +/- 0.14 mm, P < 0.05); delta max for TSM from Cap-Aer animals (0.65 +/- 0.11 mm) was not different from saline aerosol controls (0.71 +/- 0.15 mm, P = NS). We demonstrate Vmax and delta max are augmented in TSM after ovalbumin sensitization; in contrast, neurogenic inflammation caused by capsaicin has no effect on isolated TSM contractility in vitro. These data suggest that airway hyperresponsiveness in vivo that occurs in association with immunogenic or neurogenic inflammation may result from different effects of these types of inflammation on airway smooth muscle.


2019 ◽  
Vol 19 (3) ◽  
pp. 1109-1130 ◽  
Author(s):  
Marzieh Hajiaghamemar ◽  
Taotao Wu ◽  
Matthew B. Panzer ◽  
Susan S. Margulies

AbstractWith the growing rate of traumatic brain injury (TBI), there is an increasing interest in validated tools to predict and prevent brain injuries. Finite element models (FEM) are valuable tools to estimate tissue responses, predict probability of TBI, and guide the development of safety equipment. In this study, we developed and validated an anisotropic pig brain multi-scale FEM by explicitly embedding the axonal tract structures and utilized the model to simulate experimental TBI in piglets undergoing dynamic head rotations. Binary logistic regression, survival analysis with Weibull distribution, and receiver operating characteristic curve analysis, coupled with repeated k-fold cross-validation technique, were used to examine 12 FEM-derived metrics related to axonal/brain tissue strain and strain rate for predicting the presence or absence of traumatic axonal injury (TAI). All 12 metrics performed well in predicting of TAI with prediction accuracy rate of 73–90%. The axonal-based metrics outperformed their rival brain tissue-based metrics in predicting TAI. The best predictors of TAI were maximum axonal strain times strain rate (MASxSR) and its corresponding optimal fraction-based metric (AF-MASxSR7.5) that represents the fraction of axonal fibers exceeding MASxSR of 7.5 s−1. The thresholds compare favorably with tissue tolerances found in in–vitro/in–vivo measurements in the literature. In addition, the damaged volume fractions (DVF) predicted using the axonal-based metrics, especially MASxSR (DVF = 0.05–4.5%), were closer to the actual DVF obtained from histopathology (AIV = 0.02–1.65%) in comparison with the DVF predicted using the brain-related metrics (DVF = 0.11–41.2%). The methods and the results from this study can be used to improve model prediction of TBI in humans.


2001 ◽  
Vol 33 (5) ◽  
pp. S297
Author(s):  
J A. Carrithers ◽  
S W. Trappe ◽  
W J. Evans ◽  
T A. Trappe

1978 ◽  
Vol 34 (1) ◽  
pp. 173-192
Author(s):  
A.M. Glauert ◽  
A.E. Butterworth ◽  
R.F. Sturrock ◽  
V. Houba

A characteristic sequence of events has been identified by phase-contrast and electron microscopy during antibody-dependent, eosinophil-mediated damage to schistosomula of Schistosoma mansoni in vitro. Human eosinophils initially adhere to the intact schistosomulum and then, in the presence of antibody, flatten and spread very intimately over the parasite's surface. Subsequently, dense material similar to the contents of the lysosomal granules of the eosinophils appears in the extracellular space between the eosinophil and the schistosomulum, probably following fusion of the granules with the plasma membrane of the cell. Eventually all the eosinophils adhering to the parasite are completely degranulated and large amounts of the dense material are observed on the surface of the schistosomulum. This release of granular material from the eosinophils is followed by structural changes in the schistosomulum, starting with vacuolation of the inner layer of the tegument, followed by removal of the tegument, often in the form of large sheets. Subsequently the tegument disintegrates and the fragments are phagocytosed by other eosinophils which have not degranulated. Eosinophils then attach to the exposed muscle layers of the schistosomula and participate in the further degradation of the parasites by phagocytosing fragments of muscle fibres and other cellular components. This sequence of events is compared with published observations of the damage induced by various combinations of antibody, complement and effector cells in vitro, and of cell-mediated damage to schistosomula in vivo, and it is concluded that the observations described in the present paper may reflect a process of destruction of schistosomula in the immune host.


1995 ◽  
Vol 108 (12) ◽  
pp. 3795-3805 ◽  
Author(s):  
F. Schuler ◽  
L.M. Sorokin

The expression of laminin-1 (previously EHS laminin) and laminin-2 (previously merosin) isoforms by myogenic cells was examined in vitro and in vivo. No laminin alpha 2 chainspecific antibodies react with mouse tissues, 50 rat monoclonal antibodies were raised against the mouse laminin alpha 2 chain: their characterization is described here. Myoblasts and myotubes from myogenic cell lines and primary myogenic cultures express laminin beta 1 and gamma 1 chains and form a complex with a 380 kDa alpha chain identified as laminin alpha 2 by immunofluorescence, immunoprecipitation and PCR. PCR from C2C12 myoblasts and myotubes for the laminin alpha 2 chain gene (LamA2) provided cDNA sequences which were used to investigate the in vivo expression of mouse LamA2 mRNA in embryonic tissues by in situ hybridization. Comparisons were made with specific probes for the laminin alpha 1 chain gene (LamA1). LamA2 but not LamA1 mRNA was expressed in myogenic tissues of 14- and 17-day-old mouse embryos, while the laminin alpha 2 polypeptide was localized in adjacent basement membranes in the muscle fibres. In situ hybridization also revealed strong expression of the LamA2 mRNA in the dermis, indicating that laminin alpha 2 is expressed other than by myogenic cells in vivo. Immunofluorescence studies localized laminin alpha 2 in basement membranes of basal keratinocytes and the epithelial cells of hair follicles, providing new insight into basement membrane assembly during embryogenesis. In vitro cell attachment assays revealed that C2C12 and primary myoblasts adhere to laminin-1 and -2 isoforms in a similar manner except that myoblast spreading was significantly faster on laminin-2. Taken together, the data suggest that laminins 1 and 2 play distinct roles in myogenesis.


1993 ◽  
Vol 183 (1) ◽  
pp. 101-113 ◽  
Author(s):  
K. M. Gilmour ◽  
C. P. Ellington

The amplitude and time course of muscle length changes were examined in vivo in tethered, flying bumblebees Bombus lucorum. A ‘window’ was cut in the dorsal cuticle and aluminium particles were placed on the exposed dorsal longitudinal muscle fibres. Muscle oscillations were recorded using high-speed video and a high-magnification lens. The amplitude of muscle length changes was 1.9 % (s.d.=0.5 %, N=7), corresponding to the commonly quoted strain of 1–3 % for asynchronous muscle. Higher harmonics, particularly the second, were found in the muscle oscillations and in the wing movements. The second harmonic for wing movements was damped in comparison to that for muscle length changes, probably as a result of compliance in the thoracic linkage. Inclusion of the second harmonic in the driving signal for in vitro experiments on glycerinated fibres generally resulted in a decrease in the work and power, but a substantial increase was found for some fibres.


2019 ◽  
Vol 123 (5) ◽  
pp. 499-507 ◽  
Author(s):  
Xiaoling Chen ◽  
Xiaoming Luo ◽  
Daiwen Chen ◽  
Bing Yu ◽  
Jun He ◽  
...  

AbstractThe present study aimed to investigate whether arginine (Arg) promotes porcine type I muscle fibres formation via improving mitochondrial biogenesis. In the in vivo study, a total of sixty Duroc × Landrace × Yorkshire weaning piglets with an average body weight of 6·55 (sd 0·36) kg were randomly divided into four treatments and fed with a basal diet or a basal diet supplemented with 0·5, 1·0 and 1·5 % l-Arg, respectively, in a 4-week trial. Results showed that dietary supplementation of 1·0 % Arg significantly enhanced the activity of succinate dehydrogenase, up-regulated the protein expression of myosin heavy chain I (MyHC I) and increased the mRNA levels of MyHC I, troponin I1, C1 and T1 (Tnni1, Tnnc1 and Tnnt1) in longissimus dorsi muscle compared with the control group. In addition, ATPase staining analysis indicated that 1·0 % Arg supplementation significantly increased the number of type I muscle fibres and significantly decreased the number of type II muscle fibres. Furthermore, 1·0 % Arg supplementation significantly up-regulated PPAR-γ coactivator-1α (PGC-1α), sirtuin 1 and cytochrome c (Cytc) protein expressions, increased PGC-1α, nuclear respiratory factor 1 (NRF1), mitochondria transcription factor B1 (TFB1M), Cytc and ATP synthase subunit C1 (ATP5G) mRNA levels and increased mitochondrial DNA content. In the in vitro study, mitochondrial complex I inhibitor rotenone (Rot) was used. We found that Rot annulled Arg-induced type I muscle fibres formation. Together, our results provide for the first time the evidence that Arg promotes porcine type I muscle fibres formation through improvement of mitochondrial biogenesis.


1987 ◽  
Vol 127 (1) ◽  
pp. 413-426 ◽  
Author(s):  
A. J. EL HAJ ◽  
D. F. HOULIHAN

In vivo protein synthesis rates were measured in the carpopodite extensor muscle of the shore crab, Carcinus maenas, following a single, high-dose injection of [3H]phenylalanine, which stabilized specific radioactivities in the free pools. In intermoult animals the percentage of protein mass synthesized per day (the fractional rate of protein synthesis) was 1.15% day−1 for the whole extensor muscle. The small, slow-type tonic fibres in the extensor had fractional rates of protein synthesis some 2.1 times higher than those of the large, fast-type phasic fibres. Measurement of protein synthesis rates of extensor muscles from intermoult animals using an in vitro incubation over 2h gave fractional synthesis rates three times lower than those found in in vivo experiments. Compared with the intermoult animals, six- and three-fold increases in fractional synthesis rates were found in the extensor muscles from stages immediately preceding and following ecdysis, respectively. Microdissection of the muscle fibres revealed that the increased synthesis in postecdysial animals was occurring mainly at the external cuticular end of the muscle fibres. Autoradiographic analysis confirmed the cuticular end of the muscles as the major site of muscle protein synthesis. We conclude that the postecdysial increase in muscle fibre length and the associated increase in the sarcomere number is accompanied by an increase in protein synthesis in the muscles.


1992 ◽  
Vol 102 (4) ◽  
pp. 779-787 ◽  
Author(s):  
J.E. Morgan ◽  
S.E. Moore ◽  
F.S. Walsh ◽  
T.A. Partridge

The C2 muscle cell line is myogenic in vitro and has been extensively used in studies of muscle cell differentiation. Here, we have investigated the myogenicity in vivo of C2 cells implanted into suitable sites in the mouse. Large amounts of new muscle were formed when C2 cells were implanted into sites in nude mice which were undergoing regeneration following whole muscle grafting and in scaffolding of freeze-killed muscle or vicryl suture in the anterior tibial compartment. When implanted into regenerating muscle, C2 cells fused with the host muscle to form mosaic fibres; when implanted into inert sites, they formed muscle of largely donor origin. C2-derived muscle fibres appeared to become innervated, but the progression of N-CAM (neural cell adhesion molecule) isoform changes in such regenerates indicated that they did not become fully mature. Proliferating, undifferentiated cells of C2 origin form tumours in older grafts; however, this was more pronounced in the absence of competition from host muscle cells. In the short term, C2 cells can form large amounts of muscle in vivo for biochemical analysis. In addition, C2 cells are easily manipulable in vitro; genes of interest may be transfected into them prior to implantation of the cells into skeletal muscle and the effects of these genes in vivo may thus be examined.


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